Although it is not clear how decreased monoamine functions contribute to the development of depression, the current antidepressants may exert their therapeutic effects via producing secondary neuroplasticity, as well as upregulating brain-derived neurotrophic factor (BDNF) and adult hippocampal neurogenesis by increasing the number of monoamines at synaptic site1,4–6. This evidence concerns the gene BDNF and depressive symptom measurement.